Evidence map›Paper›PMID 17938216›Full record

ArticleInfection and immunity2008

Phagocytosis of Borrelia burgdorferi, the Lyme disease spirochete, potentiates innate immune activation and induces apoptosis in human monocytes.

Adriana R Cruz, Meagan W Moore, Carson J La Vake, Christian H Eggers, Juan C Salazar, Justin D Radolf

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Trial
  4. Comparative evaluation of viability assays and functional analysis ofApplied and environmental microbiology · 2026
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  7. Strain-specific immune response patterns toInfection and immunity · 2026
    Article
  8. Article
  9. Frontiers in immunology · 2026
    Article
  10. Review
  11. Article
  12. Modulation of Macrophage Redox and Apoptotic Processes toPathogens (Basel, Switzerland) · 2023
    Article
  13. Article
  14. Review
  15. Inhibition ofInternational journal of molecular sciences · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Adriana R CruzDepartment of Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-3715, USA.
Meagan W Moore
Carson J La Vake
Christian H Eggers
Juan C Salazar
Justin D Radolf
Connecticut Children's Medical Center · USUConn Health · US

Funding

ZONISAMIDE VERSUS PLACEBOM01RR006192 · NCRR · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI DRAZINIC, CAROLYN M · 1994 to 2008
$22.1M
RpoS Regulation of Borrelia burgdorferi Genes in vivoR01AI029735 · NIAID · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI CAIMANO, MELISSA J, RADOLF, JUSTIN D · 1990 to 2022
$10.7M
Treponema pallidum Outer Membrane Proteins and Transition Metal AcquisitionR01AI026756 · NIAID · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI RADOLF, JUSTIN D · 1992 to 2017
$5.1M
CUTANEOUS IMMUNE RESPONSE IN SECONDARY SYPHILISR01AI038894 · NIAID · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI RADOLF, JUSTIN D · 1996 to 2005
$2.1M
T.pallidum Membrane Immunogens and Anti-Oxidant DefenseR37AI026756 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RADOLF, JUSTIN D · 2002 to 2006
$1.8M
RpoS Regulation of Borrelia burgdorferi Genes in vivoR56AI029735 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI RADOLF, JUSTIN D · 2012 to 2012
$536k
Immunity in Early Syphillis: Pathway to HIV CoinfectionK23AI062439 · NIAID · CONNECTICUT CHILDREN'S MEDICAL CENTER · PI SALAZAR, JUAN C · 2005 to 2007
$454k
MEMBRANE PROTEINS OF TREPONEMA PALLIDUMR29AI026756 · NIAID · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI RADOLF, JUSTIN D. · 1988 to 1991
–
NCRR NIH HHS M01 RR006192NCRR NIH HHS M01RR06192NIAID NIH HHS AI-26756NIAID NIH HHS AI-29735NIAID NIH HHS AI-38894NIAID NIH HHS K23 AI062439NIAID NIH HHS K23 AI-62439NIAID NIH HHS R01 AI026756NIAID NIH HHS R01 AI029735NIAID NIH HHS R01 AI038894NIAID NIH HHS R37 AI026756NIAID NIH HHS R56 AI029735
6 · The paper itself

Abstract

We have previously demonstrated that phagocytosed Borrelia burgdorferi induces activation programs in human peripheral blood mononuclear cells that differ qualitatively and quantitatively from those evoked by equivalent lipoprotein-rich lysates. Here we report that ingested B. burgdorferi induces significantly greater transcription of proinflammatory cytokine genes than do lysates and that live B. burgdorferi, but not B. burgdorferi lysate, is avidly internalized by monocytes, where the bacteria are completely degraded within phagolysosomes. In the course of these experiments, we discovered that live B. burgdorferi also induced a dose-dependent decrease in monocytes but not a decrease in dendritic cells or T cells and that the monocyte population displayed morphological and biochemical hallmarks of apoptosis. Particularly noteworthy was the finding that apoptotic changes occurred predominantly in monocytes that had internalized spirochetes. Abrogation of phagocytosis with cytochalasin D prevented the death response. Heat-killed B. burgdorferi, which was internalized as well as live organisms, induced a similar degree of apoptosis of monocytes but markedly less cytokine production. Surprisingly, opsonophagocytosis of Treponema pallidum did not elicit a discernible cell death response. Our combined results demonstrate that B. burgdorferi confined to phagolysosomes is a potent inducer of cytosolic signals that result in (i) production of NF-kappaB-dependent cytokines, (ii) assembly of the inflammasome and activation of caspase-1, and (iii) induction of programmed cell death. We propose that inflammation and apoptosis represent mutually reinforcing components of the immunologic arsenal that the host mobilizes to defend itself against infection with Lyme disease spirochetes.

Indexed as

ApoptosisPhagocytosisBorrelia burgdorferiCells, CulturedCytokinesHumansImmunity, InnateInflammationLyme DiseaseMonocytesTranscription, GeneticTreponema pallidumCytokines

Identifiers

PMID17938216
PMCPMC2223637
OpenAlexW2110632261

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.